OBJECTIVE Coronary artery ectasia (CAE) is increasingly recognized as an active inflammatory vascular disorder rather than a benign anatomical variant. The pan-immune-inflammation value (PIV) is a novel biomarker integrating neutrophil, monocyte, platelet, and lymphocyte counts, providing a comprehensive measure of systemic inflammation. This study aimed to evaluate the association between PIV and CAE and to compare their diagnostic performance with that of conventional inflammatory indices.
METHOD In this retrospective case-control study, 17,538 patients who underwent elective coronary angiography between 2018 and 2024 were screened. A total of 228 patients with isolated CAE and 296 age-, sex-, and Body Mass Index (BMI)-matched controls with normal coronary arteries were included. Hematologic and biochemical parameters were analyzed, and inflammatory indices were calculated. Logistic regression and receiver operating characteristic (ROC) analyses were performed to identify independent predictors and assess diagnostic performance.
RESULTS Patients with CAE had significantly higher PIV levels compared to controls (801.6 [504.4–1301.8] vs. 491.8 [302.4–872.7], P < 0.001). In multivariable logistic regression, log-transformed PIV remained independently associated with CAE (odds ratio [OR]: 1.987, 95% confidence interval [CI]: 1.057–3.737, P = 0.033), along with hypertension, triglycerides, high-density lipoprotein (HDL) cholesterol, and serum creatinine. PIV demonstrated the highest discriminative ability among all inflammatory indices (area under the curve [AUC]: 0.674, 95% CI: 0.623–0.722), and correlated strongly with the Systemic Immune-Inflammation Index (SII), neutrophil-to-lymphocyte ratio (NLR), platelet-to-lymphocyte ratio (PLR), and Systemic Inflammation Response Index (SIRI) (P = 0.75–0.94).
CONCLUSION Elevated PIV levels are independently associated with CAE, reflecting the pivotal role of systemic inflammation in its pathogenesis. Given its simplicity and availability, PIV may serve as a practical adjunctive marker for identifying patients at risk of CAE, warranting validation in larger prospective studies.
Copyright © 2025 Archives of the Turkish Society of Cardiology
